[Disorders of thrombin interaction with the blood vessel wall and its inactivation by antithrombin III in experimental nephrotic syndrome].
In the experiments on white rats was conducted a comparative study of 125I-alpha-thrombin clearance and its inactivation by antithrombin III in animals of the control group and rats with the experimental nephrotic syndrome (Heymann nephritis). It was determined that alterations of thrombin binding to the vascular wall in the nephrotic syndrome induced the prolongation of the labelled enzyme half-life in the blood stream. The formation of 125I-alpha-thrombin complexes with antithrombin III was delayed in the nephrotic syndrome, that suggests the violation of mechanisms of thrombin inactivation by antithrombin III. The distortions of endothelium-mediated thrombin elimination and inactivation in the nephrotic syndrome resulted in the enzyme interaction with fibrinogen, which threatened organism by thrombosis.
Bashkov
G V
GV
D000818:Animals; D000990:Antithrombin III / Q000494:pharmacology*; D001808:Blood Vessels / Q000378:metabolism*; D004586:Electrophoresis; D005340:Fibrinogen / Q000378:metabolism; D005921:Glomerulonephritis / Q000097:blood*; D006207:Half-Life; D007457:Iodine Radioisotopes; D009404:Nephrotic Syndrome / Q000097:blood*; D051381:Rats; D013917:Thrombin / Q000032:analysis / Q000378:metabolism*; D013927:Thrombosis / Q000209:etiology
D007457:Iodine Radioisotopes; D000990:Antithrombin III; D005340:Fibrinogen; D013917:Thrombin
Narushenie vzaimodeĭstviia trombina s sosudistoĭ stenkoĭ i ego inaktivatsii antitrombinom III pri éksperimental'nom nefroticheskom sindrome.